Tuberculous constrictive pericarditis with concurrent active pulmonary tuberculous infection: a case report
Department of Cardiology, Dalin Tzu Chi General Hospital
2, Min-Sheng Road, Dalin, Chia-Yi County
Division of Cardiology, Department of Internal Medicine, National Cheng Kung University Hospital Dou-Liou Branch
345, Chuang-Ching Road, Dou-Liou, Yun-Lin County
Department of Internal Medicine, National Cheng Kung University Hospital
138, Sheng-Li Road, Tainan
Introduction: In some particular endemic area, it is not uncommon to see patients with tuberculosis pericarditis. However, it takes a period of time from tuberculous pericarditis to constrictive pericarditis. There is still no report of tuberculous constrictive pericarditis concurrent with active pulmonary TB infection in a patient without previous pulmonary TB infection history. Therefore, we reported a TB constrictive pericarditis with rare disease progress. Case presentation: We report the case of a 63-year-old Taiwanese man with tuberculous constrictive pericarditis concurrent with active pulmonary tuberculous infection presenting with progressive extremities edema, puffy face, abdominal distension and dyspnea on exertion found to be caused by right heart failure. The patient was cured by pericardial stripping and anti-tuberculosis chemotherapy. We reviewed other cases of tuberculous constrictive pericarditis from the literature and described the peculiarities of this case. Conclusions: Rapid diagnosis and treatment of constrictive pericarditis are crucial to reduce mortality. In some endemic areas, Mycobacterium tuberculosis infection should be taken into consideration during diagnostic evaluations for constrictive pericarditis. Surgical intervention is still the treatment of choice when the patient has the symptoms or signs of pericardial constriction and right heart failure. Our case is a constant reminder that active Mycobacterium tuberculosis infection does present itself with uncommon presentations.
Constrictive pericarditis is a process of chronic fibrous
thickening of the pericardium, which is frequently
accompanied with calcification and prevents the diastolic
filling of the heart, reducing venous return and lowering
output [1,2]. Pericardial constriction is resulted from the
chronic inflammation of the pericardium, which leads to
pericardial scarring, thickening, fibrosis, and calcification
. Many etiologies have been identified, such as
idiopathic chronic pericarditis, infection, after cardiac
surgery, and mediastinal radiotherapy [2,4,5].
Mycobaterium tuberculosis is the most common cause of
constrictive pericarditis in endemic area . The definite
diagnosis is based on one of the following criteria:
(1) positive Mycobaterium tuberculosis culture from
pericardial effusion or tissue, (2) positive acid-fast stain
bacilli or typical caseous granuloma on pericardial biopsy
specimen, or (3) positive tuberculosis polymerase chain
reaction in the pericardial biopsy specimen .
A 63-year-old Taiwanese male patient was presented in
October 2006 with progressive extremities edema, puffy
face, abdominal distension and dyspnea on exertion for
2 weeks. There was no chest discomfort, orthopnea or
paroxysmal nocturnal dyspnea. He did not have symptoms
of cough, fever, foamy urine, or body weight loss. He had
diabetes mellitus for years, which was well controlled with
insulin. Physical examination revealed generalized pitting
edema with elevated jugular venous pressure, positive
Kussmauls sign, and hepatomegaly. Bilateral pleural
effusion, patchy infiltration at right middle lung field, and
cardiomegaly were noted on chest X-ray (Figure 1A).
Pneumonia was diagnosed by the chest specialist first in
our out-patient department, and the patient was transferred
to the emergency department (ED) due to the diagnosis of
pneumonia and severe dyspnea. Thoracentesis, done in
ED, revealed a transudate as the level of total protein and
lactate dehydrogenase (LDH) of the pleural fluid were
2.800 mg/dL and 79 mg/dL, respectively, while serum
protein was 7.700 mg/dL and serum LDH was 190 mg/dL.
Chest computed tomography scan also revealed thickened
pericardium, up to 3 mm in diameter, minimal amount of
pericardial effusion, a patchy fibrotic infiltration with
bronchiectasis over the right upper lung, irregular thickening
of the right intermediate bronchus, and obstruction of the
right middle lung bronchus with consolidation and
atelectasis of right middle lobe (Figure 1B). There were several
lymph nodes, up to 2.2 cm in size, in right paratracheal,
pretracheal, subcarinal and left prevascular areas.
After treatment with diuretics, the peripheral edema
improved significantly, but the patient still complained of
severe dyspnea on exertion during the hospitalization.
Echocardiograms showed thickened pericardium, especially
over the right atrium, and small amount of pericardial
effusion. The left ventricular wall motion was normal.
However, there were limited right atrial wall motion and
distended inferior vena cava with blunted respiratory
variation. Under the impression of right heart failure due
to constrictive pericarditis, the patient underwent cardiac
catheterization. The hemodynamic studies (Figure 2A, 2B,
Figure 1. Image studies of the patient. (A) A chest X-ray; (B) a CT scan of the thorax showing thickened pericardium with areas
of calcification, and bilateral pleural effusions.
Figure 2. Pressure tracing of right-sided heart catheterization. (A) Right atrial pressure tracing; (B) right ventricular pressure;
(C) simultaneous ventricular pressure tracing.
and 2C) showed right atrium pressure 24/22 mmHg,
pulmonary capillary wedge pressure 23 mmHg, prominent
x and y descent in right atrial pressure tracings,
dip-andplateau pattern in the right ventricular diastolic pressure
tracings. There was equalization of the end-diastolic
pressures between right and left ventricles (24 mmHg).
Because of the diagnosis of constrictive pericarditis
complicated with right heart failure, surgical operation
for pericardial stripping was performed. Operative
findings included markedly thickened pericardium and
enlarged mediastinal lymph nodes. The postoperative
course was uneventful with improvement of heart
function. Pathology of the removed pericardium showed
obvious granulomatous changes with caseous necrosis.
Only one sample of sputum specimen was collected on the
operation day with vigorous humidifier using normal
saline for several days, which was positive for acid-fast
stain. The sputum culture gave positive result of
Mycobacterium tuberculosis four weeks later. The patient was put on
quadruple anti-tuberculosis chemotherapy and remains
free from symptoms of heart failure.
Persistent tuberculous pericarditis will lead to pericardial
constriction due to chronic granulomatous inflammation
of the pericardium with subsequent deposition of
fibrinous strands, demonstrable on echocardiography .
Use of corticosteroid as an adjuvant therapy has been
recommended for patients with tuberculous pericarditis
and in the presence of large amount of pericardial or
pleural effusion to suppress inflammation and reduce
effusion. However, corticosteroids may aggravate the
immunity of a compromised host, especially in the elderly
[4,9,10]. Thus, the benefit of corticosteroids as adjuvant
therapy in tuberculous pericarditis remains uncertain.
Corticosteroids were not used in this patient, because
only a small amount of pericardial effusion was detected
by echocardiography initially and during follow-up period
after operation. Moreover, anti-tuberculosis chemotherapy
is still the cornerstone of the treatment for tuberculous
pericarditis. In the endemic area, six-month
anti-tuberculosis chemotherapy is recommended. The initial phase
should consist of 2 months of isoniazid, rifampicin,
pyrazinamide, and ethambutol. The preferred
continuation phase consists of isoniazid and rifampicin given for
4 months .
In the chronic stage of tuberculous constrictive pericarditis,
pericardial decortication with wide resection of both the
visceral and the parietal pericardium, remains the definitive
treatment . However, there are no clear-cut determinants
for surgical intervention when managed at the early
stage. Yang et al. once reported that decision largely
depended on the clinical symptoms of cardiac temponade,
progression of heart failure, and constriction that lead to
jugular vein engrossment . They highlighted the
importance of pursuing early pericardiectomy, rather than
pericardiocentesis and window placement, to achieve
sustained relief of symptoms in patients with advanced
The diagnosis of tuberculous constrictive pericarditis in
the current patient was confirmed by pathological
findings. The patient did not suffer from any airway
symptoms, even though atypical, for pulmonary
tuberculosis, but was later verified by a positive sputum acid-fast
stain and culture of Mycobacterium tuberculosis. It was not
uncommon to see patients with tuberculous pericarditis,
either effusive or constrictive, especially in endemic area,
but our past experiences were that tuberculous constrictive
pericarditis occurred much later after active tuberculous
pulmonary infection or ineffective therapy of the
pulmonary infection. There was no reported case of
tuberculous constrictive pericarditis with concurrent active
pulmonary tuberculosis. Our case is a constant reminder
that active Mycobacterium tuberculosis infection does present
itself with uncommon presentations.
Rapid diagnosis and treatment of constrictive pericarditis
are crucial to reduce mortality. In some endemic areas,
Mycobacterium tuberculosis infection should be taken into
consideration during diagnostic evaluations for
constrictive pericarditis. Surgical intervention is still the treatment
of choice when the patient has the symptoms or signs of
pericardial constriction and right heart failure.
List of abbreviations
ED, emergency department; LDH, lactate dehydrogenase.
Written informed consent was obtained from the patient
for publication of this case report and all accompanying
images. A copy of the written consent is available for
review by the Editor-in-chief of this journal.
The authors declare that they have no competing interests.
YWL was in charge of the patient, followed up the case and
wrote the initial manuscript. HRT, and WHL contributed
to the clinical work-up of the patient, including
echocardiography and cardiac catheterization study. LJL and JHC
carried out a review of the manuscript and made the final
changes before submission.